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Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.


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TL;DR: The challenges and opportunities in developmental physiology outlined by a symposium at the 2014 American Physiological Society Intersociety Meeting: Comparative Approaches to Grand Challenges in Physiology as mentioned in this paper.
Abstract: This review explores challenges and opportunities in developmental physiology outlined by a symposium at the 2014 American Physiological Society Intersociety Meeting: Comparative Approaches to Grand Challenges in Physiology. Across animal taxa, adverse embryonic/fetal environmental conditions can alter morphological and physiological phenotypes in juveniles or adults, and capacities for developmental plasticity are common phenomena. Human neonates with body sizes at the extremes of perinatal growth are at an increased risk of adult disease, particularly hypertension and cardiovascular disease. There are many rewarding areas of current and future research in comparative developmental physiology. We present key mechanisms, models, and experimental designs that can be used across taxa to investigate patterns in, and implications of, the development of animal phenotypes. Intraspecific variation in the timing of developmental events can be increased through developmental plasticity (heterokairy), and could provide the raw material for selection to produce heterochrony — an evolutionary change in the timing of developmental events. Epigenetics and critical windows research recognizes that in ovo or fetal development represent a vulnerable period in the life history of an animal, when the developing organism may be unable to actively mitigate environmental perturbations. ‘Critical windows’ are periods of susceptibility or vulnerability to environmental or maternal challenges, periods when recovery from challenge is possible, and periods when the phenotype or epigenome has been altered. Developmental plasticity may allow survival in an altered environment, but it also has possible long-term consequences for the animal. “Catch-up growth” in humans after the critical perinatal window has closed elicits adult obesity and exacerbates a programmed hypertensive phenotype (one of many examples of “fetal programing”). Grand challenges for developmental physiology include integrating variation in developmental timing within and across generations, applying multiple stressor dosages and stressor exposure at different developmental timepoints, assessment of epigenetic and parental influences, developing new animal models and techniques, and assessing and implementing these designs and models in human health and development.

47 citations

Journal ArticleDOI
TL;DR: The presence of specific cellular signaling pathways or tissue-specific factors underlying the establishment, maintenance, and redirection of gene expression patterns in the tissues involved in adventitious root formation could be crucial for cell fate switch and for the control of age-dependent cellular plasticity.
Abstract: Cellular plasticity refers, among others, to the capability of differentiated cells to switch the differentiation process and acquire new fates. One way by which plant cell plasticity is manifested is through de novo regeneration of organs from somatic differentiated cells in an ectopic location. However, switching the developmental program of adult cells prior to organ regeneration is difficult in many plant species, especially in forest tree species. In these species, a decline in the capacity to regenerate shoots, roots or embryos from somatic differentiated cells is associated with tree age and maturation. The decline in the ability to form adventitious roots from stem cuttings is one of the most dramatic effects of maturation, and has been the subject of investigations on the basic nature of the process. Cell fate switches, both in plants and animals, are characterized by remarkable changes in the pattern of gene expression, as cells switch from the characteristic expression pattern of a somatic cell to a new one directing a new developmental pathway. Therefore, determining the way by which cells reset their gene expression pattern is crucial to understand cellular plasticity. The presence of specific cellular signalling pathways or tissue-specific factors underlying the establishment, maintenance and redirection of gene expression patterns in the tissues involved in adventitious root formation could be crucial for cell fate switch and for the control of age-dependent cellular plasticity.

47 citations

Journal ArticleDOI
TL;DR: The concept of developmental phenotypic switching should be expanded to include sufficient plasticity allowing subsequent correction resulting in the normal adult phenotype.
Abstract: The prevalent view of developmental phenotypic switching holds that phenotype modifications occurring during critical windows of development are "irreversible" - that is, once produced by environmental perturbation, the consequent juvenile and/or adult phenotypes are indelibly modified. Certainly, many such changes appear to be non-reversible later in life. Yet, whether animals with switched phenotypes during early development are unable to return to a normal range of adult phenotypes, or whether they do not experience the specific environmental conditions necessary for them to switch back to the normal range of adult phenotypes, remains an open question. Moreover, developmental critical windows are typically brief, early periods punctuating a much longer period of overall development. This leaves open additional developmental time for reversal (correction) of a switched phenotype resulting from an adverse environment early in development. Such reversal could occur from right after the critical window "closes," all the way into adulthood. In fact, examples abound of the capacity to return to normal adult phenotypes following phenotypic changes enabled by earlier developmental plasticity. Such examples include cold tolerance in the fruit fly, developmental switching of mouth formation in a nematode, organization of the spinal cord of larval zebrafish, camouflage pigmentation formation in larval newts, respiratory chemosensitivity in frogs, temperature-metabolism relations in turtles, development of vascular smooth muscle and kidney tissue in mammals, hatching/birth weight in numerous vertebrates,. More extreme cases of actual reversal (not just correction) occur in invertebrates (e.g., hydrozoans, barnacles) that actually 'backtrack' along normal developmental trajectories from adults back to earlier developmental stages. While developmental phenotypic switching is often viewed as a permanent deviation from the normal range of developmental plans, the concept of developmental phenotypic switching should be expanded to include sufficient plasticity allowing subsequent correction resulting in the normal adult phenotype.

46 citations

Journal ArticleDOI
TL;DR: Examination of expression patterns of PSD‐95 and SynGAP genes from embryonic stages to adult using lacZ (β‐galactosidase) marker gene knock‐in mice supports the model that synaptic signalling complexes are heterogeneous and individual components show temporal and spatial specificity during development.
Abstract: Patterns of neural activity mediated by N-methyl-D-aspartate (NMDA) receptors are known to play important roles in development of the central nervous system. However, the signalling pathways downstream from NMDA receptors that are critical for normal neuronal development are not yet clearly understood. NMDA receptors interact with various signalling proteins via scaffolding proteins, which are important in adult neuronal and behavioural plasticity. For example, the NR2B subunits of the NMDA receptor interact with postsynaptic density 95 (PSD-95), which in turn binds to synaptic ras GTPase-activating protein (SynGAP). Interestingly, the developmental phenotype of mice carrying null mutations in these genes differ. NR2B and SynGAP homozygote mice die within the first week of birth whereas PSD-95 homozygote mice survive to adulthood. We therefore examined the expression patterns of PSD-95 and SynGAP genes from embryonic stages to adult using lacZ (beta-galactosidase) marker gene knock-in mice. Dramatic changes of expression were observed throughout development in brain and other tissues. Although SynGAP binds PSD-95, both genes had distinct, as well as overlapping expression. SynGAP expression peaked at times of synaptogenesis and developmental plasticity in contrast to PSD-95, which was expressed throughout the brain from early embryonic stages. Furthermore, SynGAP showed a more spatially restricted pattern as illustrated by its restriction to forebrain in contrast to PSD-95, which was also found in mid- and hindbrain. These data support the model that synaptic signalling complexes are heterogeneous and individual components show temporal and spatial specificity during development.

46 citations

Journal ArticleDOI
TL;DR: Comparison of populations of Drosophila melanogaster from environments with relatively high and relatively low variance in temperature among generations indicates that selection favors plasticity of thermal tolerances equally in these populations.

46 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202316
202244
202172
202076
201953
201864